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. Author manuscript; available in PMC: 2014 Feb 1.
Published in final edited form as: Trends Cardiovasc Med. 2012 Dec 13;23(2):33–38. doi: 10.1016/j.tcm.2012.08.008

Figure 4. Potential Model of Kinase Dependent Regulation of Cx43 Targeting.

Figure 4

Cx43 is synthesized in the rough endoplasmic reticulum (A), transported to the Golgi where monomers (B) oligomerize into connexons or hemi-channels (C), and then targeted to the intercalated disc through a mechanism that is thought to utilize microtubules and actin (D). Panel A. Under normal physiological conditions, the balance of activity between CK1δ and PP1 and PP2A favors directed transport of phosphorylated connexons (D) to gap junction plaques within junctional membrane (E), rather than targeting of non-phosphorylated connexons (F) to non-junctional membrane (G). Panel B. Under conditions where CK1δ activity greatly exceeds phosphatase activity, or is mimicked by pseudo-phosphorylation of Cx43 at CK1δ consensus sites (Cx43-S3E), targeting to junctional membrane is enhanced. Panel C. Under conditions where phosphatase activity exceeds kinase activity, or is mimicked by introduction of non-phosphorylatable residues at CK1δ consensus sites (Cx43-S3A), connexons are no longer preferentially targeted to junctional membrane, resulting in lateralization and early degradation.